Cardiomyocyte-Restricted Deletion of PPARβ/δ in PPARα-Null Mice Causes Impaired Mitochondrial Biogenesis and Defense, but No Further Depression of Myocardial Fatty Acid Oxidation
Figure 2
Cardiac pathology and survival rate. (a) Cardiac hypertrophy was estimated by heart weight/body weight ratio. (b) Transcript expression levels of ANF in α-MyHC-Cre and CR-Pd/Pa-null hearts. (c) Assessment of cardiac ultrastructure by Transmission Electron Microscopy (TEM): representative images are shown of heart sections from α-MyHC-Cre, PPARα −/−, CR-PPARβ/δ −/−, and CR-Pd/Pa-null mice at the age of 35 weeks (image magnification: 12,000x). Arrows indicate lipid droplet. (d) Kaplan-Meier survival curves: survival rates of mice from α-MyHC-Cre, CR-PPARβ/δ −/−, CR-Pd/Pa-null, and control groups after 15 months were analyzed by the log-rank test (CR-PPARβ/δ −/− or CR-Pd/Pa versus α-MyHC-Cre, ).
